Caregiver sensitivity moderates effects of gestational inflammation on child ADHD symptoms.
L’essentiel
Increased inflammation during pregnancy may increase the risk for child psychopathology, though prospective data remain preliminary. Child symptoms of attention-deficit/hyperactivity disorder (ADHD) are particularly important due to ADHD's role as an early precursor of many later forms of externalizing and internalizing problems. Despite strong theories surrounding the ways in which pre- and postnatal environmental factors may interact in the prediction of child risk, few studies have examined how the postnatal social environment moderates prenatal effects. This study examined whether gestational inflammation was prospectively related to ADHD symptoms and whether this association was moderated by postnatal caregiving behaviors. Data came from a prospective cohort of pregnant individuals and their offspring (N = 302). Second trimester inflammation was assessed in maternal plasma using a comprehensive panel of cytokines. ADHD symptoms were assessed at 36 months of age using parent-report and clinician ratings. Observer ratings of maternal sensitive caregiving behaviors were assessed when infants were 6 months old. The effect of gestational inflammation on child ADHD symptoms was moderated by maternal sensitive caregiving during infancy. Increased inflammation during pregnancy was associated with greater child ADHD symptoms only when children experienced lower levels of maternal sensitivity. Early sensitive caregiving appears to buffer children against the negative effects of gestational inflammation. Interventions that decrease gestational inflammation and those that support early caregiver-child relationships may both be effective at reducing child ADHD risk.
Synthèse détaillée
Résumé original
Increased inflammation during pregnancy may increase the risk for child psychopathology, though prospective data remain preliminary. Child symptoms of attention-deficit/hyperactivity disorder (ADHD) are particularly important due to ADHD's role as an early precursor of many later forms of externalizing and internalizing problems. Despite strong theories surrounding the ways in which pre- and postnatal environmental factors may interact in the prediction of child risk, few studies have examined how the postnatal social environment moderates prenatal effects. This study examined whether gestational inflammation was prospectively related to ADHD symptoms and whether this association was moderated by postnatal caregiving behaviors. Data came from a prospective cohort of pregnant individuals and their offspring (N = 302). Second trimester inflammation was assessed in maternal plasma using a comprehensive panel of cytokines. ADHD symptoms were assessed at 36 months of age using parent-report and clinician ratings. Observer ratings of maternal sensitive caregiving behaviors were assessed when infants were 6 months old. The effect of gestational inflammation on child ADHD symptoms was moderated by maternal sensitive caregiving during infancy. Increased inflammation during pregnancy was associated with greater child ADHD symptoms only when children experienced lower levels of maternal sensitivity. Early sensitive caregiving appears to buffer children against the negative effects of gestational inflammation. Interventions that decrease gestational inflammation and those that support early caregiver-child relationships may both be effective at reducing child ADHD risk.